migraine n : a severe recurring vascular headache; occurs more frequently in women than men [syn: megrim, sick headache, hemicrania]

English

Pronunciation

• mī'grān, /ˈmaɪɡreɪn/, /"maIgreIn/

  Rhymes: -aɪɡreɪn

Noun

1. A severe, disabling headache, usually affecting only one side of the head, and often accompanied by nausea, vomiting, photophobia and visual disturbances.

   He had a headache so bad that he wished he was dead, but it was the sort of migraine that promised him he would continue to suffer but not die.

   After consuming too much coffee everyday for six weeks, she got severe migraines that would last up until 47 minutes after her first cup of coffee.

Translations

Synonyms

• hemicrania
• megrim
• sick headache

Derived terms

• migraineur
• migrainous

this the disorder Migraine is a neurological syndrome that can cause a wide range of symptoms during an attack. The most commonly thought of symptom is headache.

It is widespread in the population. In the U.S., 18% of women and 6% of men report having had at least one migraine episode in the previous year, with seriousness ranging from an annoyance to a life-threatening and/or daily experience.

Overview

Usually migraine causes episodes of severe or moderate headache (which is often one-sided and pulsating) lasting from four to 72 hours, accompanied by gastrointestinal upsets, such as nausea and vomiting, and a heightened sensitivity to bright lights (photophobia) and noise (hyperacusis). Approximately one third of people who experience migraine get a preceding aura, in which a patient senses a strange light or unpleasant smell.

The word migraine is French in origin and comes from the Greek hemicrania, as does the Old English term megrim. Literally, hemicrania means "half (the) head".

Migraines' secondary characteristics are inconsistent. Triggers precipitating a particular episode of migraine vary widely. The efficacy of the simplest treatment, applying warmth or coolness to the affected area of the head, varies between persons, sometimes worsening the migraine. A particular migraine rescue drug may sometimes work and sometimes not work in the same patient. Some migraine types don't have pain or may manifest symptoms in parts of the body other than the head.

Available evidence suggests that migraine pain is one symptom of several to many disorders of the serotonergic control system, a dual hormone-neurotransmitter with numerous types of receptors. Two disorders — classic migraine with aura (MA, STG) and common migraine without aura (MO, STG) — have been shown to have a genetic factor. Studies on twins show that genes have a 60 to 65% influence on the development of migraine (PMID 10496258 and PMID 10204850 ). Additional migraine types are suspected and could be proven to be genetic. Migraine understood as several or many disorders could explain the inconsistencies, especially if a single patient has more than one genetic type.

However, still other migraine types might be functionally acquired due to hormone organ disease or injury. Three quarters of adult migraine patients are female, although pre-pubertal migraine affects approximately equal numbers of boys and girls. This reveals the strong correlation to hormonal cycling and hormonal-related causes or triggers. Hormonal migraine is a likely consequence of periodically falling hormone levels causing reduction in protein biosynthesis of metabolic components including intestinal tract serotonin. Migraine famously disappears during pregnancy in a substantial number of sufferers.

Classification

Migraines have been classified by the International Headache Society which periodically revises their classification.

Defining severity of pain

In addition to classifying the type of headache, the International Headache Society defines intensity of pain on a verbal 4 point scale:

• 0 no pain
• 1 mild pain 'does not interfere with usual activities'
• 2 moderate pain 'inhibits, but does not wholly prevent usual activities'
• 3 severe pain 'prevents all activities'

Migraine without aura

This is the most commonly seen form of migraine; patients who primarily suffer from migraine without aura may also have attacks of migraine with aura. According to the International Classification of Headache Disorders and about 60% of them suffer from menstrual migraines.

• There are two types of menstrual migraine – Menstrually Related Migraine (MRM) and Pure Menstrual Migraine (PMM)

• MRM is a headache of moderate-to-severe pain intensity that happens around the time of a woman’s period and at other times of the month as well.

• PMM is similar in every respect but only occurs around the time of a woman’s period.

• The exact causes of menstrual migraine are uncertain but evidence suggest there may be a link between menstruation and migraine due to the drop in estrogen levels that normally occurs right before the period starts.

• Menstrual migraine has been reported to be more likely to occur during a five-day window, from two days before to two days after menstruation.

When compared with migraines that occur at other times of the month, menstrual migraines have been reported to

• Last longer—up to 72 hours

• Be more severe

• Occur more often with nausea and vomiting

Signs and symptoms

The signs and symptoms of migraine vary among patients. Therefore, what a patient experiences before, during and after an attack cannot be defined exactly. The four phases of a migraine attack listed below are common but not necessarily experienced by all migraine sufferers. Additionally, the phases experienced and the symptoms experienced during them can vary from one migraine attack to another in the same migraineur:

1. The prodrome, which occurs hours or days before the headache.
2. The aura, which immediately precedes the headache.
3. The pain phase, also known as headache phase.
4. The postdrome.

Prodrome phase

Prodromal symptoms occur in 40 to 60% of migraineurs (migraine sufferers). This phase may consist of altered mood, irritability, depression or euphoria, fatigue, yawning, excessive sleepiness, craving for certain food (e.g. chocolate), stiff muscles (especially in the neck), constipation or diarrhea, increased urination, and other vegetative symptoms. These symptoms usually precede the headache phase of the migraine attack by several hours or days, and experience teaches the patient or observant family how to detect that a migraine attack is near.

Aura phase

For the 20–30% of individuals who suffer migraine with aura, this aura comprises focal neurological phenomena that precede or accompany the attack. They appear gradually over 5 to 20 minutes and generally last fewer than 60 minutes. The headache phase of the migraine attack usually begins within 60 minutes of the end of the aura phase, but it is sometimes delayed up to several hours, and it can be missing entirely. Symptoms of migraine aura can be visual, sensory, or motor in nature.

Visual aura is the most common of the neurological events. There is a disturbance of vision consisting usually of unformed flashes of white and/or black or rarely of multicolored lights (photopsia) or forma­tions of dazzling zigzag lines (scintillating scotoma; often arranged like the battlements of a castle, hence the alternative terms "fortification spectra" or "teichopsia"). Some patients complain of blurred or shimmering or cloudy vision, as though they were look­ing through thick or smoked glass, or, in some cases, tunnel vision and hemianopsia. The somatosensory aura of migraine consists of digitolingual or cheiro-oral paresthesias, a feeling of pins-and-needles experienced in the hand and arm as well as in the ipsilateral nose-mouth area. Paresthesia migrate up the arm and then extend to involve the face, lips and tongue.

Other symptoms of the aura phase can include auditory or olfactory hallucinations, temporary dysphasia, vertigo, tingling or numbness of the face and extremities, and hypersensitivity to touch.

Pain phase

The typical migraine headache is unilateral, throbbing, moderate to severe and can be aggravated by physical activity. Not all of these features are necessary. The pain may be bilateral at the onset or start on one side and become generalized, and 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 and 72 hours in adults and 1 and 48 hours in children. The frequency of attacks is extremely variable, from a few in a lifetime to several times a week, and the average migraineur experiences from one to three headaches a month. The head pain varies greatly in intensity. The pain of migraine is invariably accompanied by other features. Nausea occurs in almost 90 percent of patients, while vomiting occurs in about one third of patients. Many patients experience sensory hyperexcitability manifested by photophobia, phonophobia, osmophobia and seek a dark and quiet room. Blurred vision, nasal stuffiness, diarrhea, polyuria, pallor or sweating may be noted during the headache phase. There may be localized edema of the scalp or face, scalp tenderness, prominence of a vein or artery in the temple, or stiffness and tenderness of the neck. Impairment of concentration and mood are common. Lightheadedness, rather than true vertigo and a feeling of faintness may occur. The extremities tend to be cold and moist.

Postdrome phase

The patient may feel tired, "washed out", irritable, or listless and may have impaired concentration, scalp tenderness or mood changes. Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise. Often, some of the minor headache phase symptoms may continue, such as loss of appetite, photophobia, and lightheadedness. On some patients, a 5 to 6 hour nap may reduce the pain, but slight headaches may still occur when standing or sitting quickly. Normally these symptoms go away after a good night's rest.

Diagnosis

Migraines are underdiagnosed and misdiagnosed. The diagnosis of migraine without aura, according to the International Headache Society, can be made according to the following criteria, the "5, 4, 3, 2, 1 criteria":

• 5 or more attacks
• 4 hours to 3 days in duration
• 2 or more of - unilateral location, pulsating quality, moderate to severe pain, aggravation by or avoidance of routine physical activity
• 1 or more accompanying symptoms - nausea and/or vomiting, photophobia, phonophobia

For migraine with aura, only two attacks are required to justify the diagnosis.

The mnemonic POUNDing (Pulsating, duration of 4–72 hOurs, Unilateral, Nausea, Disabling) can help diagnose migraine. If 4 of the 5 criteria are met, then the positive likelihood ratio for diagnosing migraine is 24.

The presence of either disability, nausea or sensitivity, can diagnose migraine with:

• sensitivity of 81%
• specificity of 75%

Pathophysiology

Migraines were once thought to be initiated exclusively by problems with blood vessels. The vascular theory of migraines is now considered secondary to brain dysfunction and claimed to have been discredited by others.

The effects of migraine may persist for some days after the main headache has ended. Many sufferers report a sore feeling in the area where the migraine was, and some report impaired thinking for a few days after the headache has passed.

Migraine headaches can be a symptom of hypothyroidism.

Depolarization theory

A phenomenon known as cortical spreading depression can cause migraines. In cortical spreading depression, neurological activity is depressed over an area of the cortex of the brain. This situation results in the release of inflammatory mediators leading to irritation of cranial nerve roots, most particularly the trigeminal nerve, which conveys the sensory information for the face and much of the head.

This view is supported by neuroimaging techniques, which appear to show that migraine is primarily a disorder of the brain (neurological), not of the blood vessels (vascular). A spreading depolarization (electrical change) may begin 24 hours before the attack, with onset of the headache occurring around the time when the largest area of the brain is depolarized. A French study in 2007, using the Positron Emission Tomography (PET) technique identified the hypothalamus as being critically involved in the early stages.

Vascular theory

Migraines can begin when blood vessels in the brain contract and expand inappropriately. This may start in the occipital lobe, in the back of the brain, as arteries spasm. The reduced flow of blood from the occipital lobe triggers the aura that some individuals who have migraines experience because the visual cortex is in the occipital area. However this figure — the lifetime prevalence — does not provide a very clear picture of how many patients there are with active migraine at any one time. Typically, therefore, the burden of migraine in a population is assessed by looking at the one-year prevalence — a figure that defines the number of patients who have had one or more attacks in the previous year. The third figure, which helps to clarify the picture, is the incidence — this relates to the number of first attacks occurring at any given age and helps understanding of how the disease grows and shrinks over time. Based on the results of a number of studies, one year prevalence of migraine ranges from 6–15% in adult men and from 14–35% in adult women. There is then a rapid growth in incidence amongst girls occurring after puberty, which continues throughout early adult life. By early middle age, around 25% of women experience a migraine at least once a year, compared with fewer than 10% of men. After menopause, attacks in women tend to decline dramatically, so that in the over 70s there are approximately equal numbers of male and female sufferers, with prevalence returning to around 5%. Incidence figures show that the excess of migraine seen in women of reproductive age is mainly due to migraine without aura.

There is a strong relationship between age, gender and type of migraine.

Geographical differences in migraine prevalence are not marked. Studies in Asia and South America suggest that the rates there are relatively low, but they do not fall outside the range of values seen in European and North American studies.

Triggers

A migraine trigger is any factor that, on exposure or withdrawal, leads to the development of an acute migraine headache. Triggers may be categorized as behavioral, environmental, infectious, dietary, chemical, or hormonal. In the medical literature, these factors are known as 'precipitants.'

Migraine attacks may be triggered by:

• Allergic reactions
• Bright lights, loud noises, and certain odors or perfumes
• Physical or emotional stress
• Changes in sleep patterns
• Smoking or exposure to smoke
• Skipping meals
• Dehydration
• Alcohol or caffeine
• Menstrual cycle fluctuations, birth control pills
• Tension headaches
• Foods containing tyramine (red wine, aged cheese, smoked fish, chicken livers, figs, and some beans), monosodium glutamate or nitrates (preserved meats)
• Other foods such as chocolate, nuts, peanut butter, avocado, banana, citrus, onions, dairy products, and fermented or pickled foods.

Sometimes the migraine occurs with no apparent "cause". The trigger theory supposes that exposure to various environmental factors precipitates, or triggers, individual migraine episodes. Migraine patients have long been advised to try to identify personal headache triggers by looking for associations between their headaches and various suspected trigger factors and keeping a "headache diary" recording migraine incidents and diet to look for correlations in order to avoid trigger foods. It must be mentioned, that some trigger factors are quantitative in nature, i.e., a small block of dark chocolate may not cause a migraine, but half a slab of dark chocolate almost definitely will, in a susceptible person. In addition, being exposed to more than one trigger factor simultaneously will more likely cause a migraine, than a single trigger factor in isolation, e.g., drinking and eating various known dietary trigger factors on a hot, humid day, when feeling stressed and having had little sleep will probably result in a migraine in a susceptible person, but consuming a single trigger factor on a cool day, after a good night's rest with minimal environmental stress may mean that the sufferer will not develop a migraine after all. Migraines can be complex to avoid, but by keeping an accurate migraine diary and making suitable lifestyle changes can have a very positive effect on the sufferer's quality of life. Some trigger factors are virtually impossible to avoid, e.g. the weather or emotions, but by limiting the avoidable trigger factors, the unavoidable ones may have less of an impact on the sufferer.

Food

A 2005 literature review found that the available information about dietary trigger factors relies mostly on the subjective assessments of patients. Some suspected dietary trigger factors appear to genuinely promote or precipitate migraine episodes, but many other suspected dietary triggers have never been demonstrated to trigger migraines. The review authors found that alcohol, caffeine withdrawal, and missing meals are the most important dietary migraine precipitants, that dehydration deserved more attention, and that some patients report sensitivity to red wine. Little or no evidence associated notorious suspected triggers like chocolate, cheese, histamine, tyramine, nitrates, or nitrites with migraines. The artificial sweetener aspartame has not been shown to trigger headache, but in a large and definitive study monosodium glutamate (MSG) in large doses (2.5 grams) was associated with adverse symptoms including headache more often than was placebo. The review authors also note that while general dietary restriction has not been demonstrated to be an effective migraine therapy, it is beneficial for the individual to avoid what has been a definite cause of the migraine.

The National Headache Foundation has a specific list of triggers based on the tyramine theory, detailing allowed, with caution and avoid triggers.

Weather

Several studies have found some migraines are triggered by changes in weather. One study noted 62% of the subjects thought weather was a factor but only 51% were sensitive to weather changes. Among those whose migraines did occur during a change in weather, the subjects often picked a weather change other than the actual weather data recorded. Most likely to trigger a migraine were, in order:

1. Temperature mixed with humidity. High humidity plus high or low temperature was the biggest cause.
2. Significant changes in weather
3. Changes in barometric pressure

Another study examined the effects of warm chinook winds on migraines, with many patients reporting increased incidence of migraines immediately before and/or during the chinook winds. The number of people reporting migrainous episodes during the chinook winds was higher on high-wind chinook days. The probable cause was thought to be an increase in positive ions in the air.

Head position

One study suggests that migraines can be triggered by the head being held downwards for an extended period, as when washing hair in a basin.

Treatment

Conventional treatment focuses on three areas: trigger avoidance, symptomatic control, and preventive drugs. Patients who experience migraines often find that the recommended treatments are not 100% effective at preventing migraines, and sometimes may not be effective at all.

Children and adolescents, are often first given drug treatment, but the value of diet modification should not be overlooked. The simple task of starting a diet journal to help modify the intake of trigger foods like hot dogs, chocolate, cheese and ice cream could help alleviate symptoms

Abortive treatment

Migraine sufferers usually develop their own coping mechanisms for the pain of a migraine attack. Hot or cold water applied to the head, resting in a dark and silent room or ingesting caffeine at an appropriate time may be as helpful as medication for some patients.

For patients who have been diagnosed with recurring migraines, migraine abortive medications can be used to treat the attack, and may be more effective if taken early, losing effectiveness once the attack has begun. Treating the attack at the onset can often abort it before it becomes serious, and can reduce the near-term frequency of subsequent attacks.

Paracetamol or Non-steroidal anti-inflammatory drug (NSAIDs)

The first line of treatment is over-the-counter abortive medication.

• Regarding non-steroidal anti-inflammatory drugs, a randomized controlled trial found that naproxen can abort about one third of migraine attacks, which was 5% less than the benefit of sumatriptan.
• Paracetamol, at a dose of 1000 mg, benefited over half of patients with mild or moderate migraines in a randomized controlled trial.
• Simple analgesics combined with caffeine may help. During a migraine attack, emptying of the stomach is slowed, resulting in nausea and a delay in absorbing medication. Caffeine has been shown to partially reverse this effect, and probably accounts for its benefit. Excedrin is an example of an aspirin with caffeine product. Caffeine is recognized by the U.S. FDA as an Over The Counter Drug (OTC) treatment for migraine.

Patients themselves often start off with paracetamol (known as acetaminophen in the USA), aspirin, ibuprofen, or other simple analgesics that are useful for tension headaches. OTC drugs may provide some relief, although they are typically not effective for most sufferers. It is one of doctors' practical diagnoses of migraine head pain when patients say typical OTC drugs "won't touch it".

Analgesics combined with antiemetics

Anti-emetics by mouth may help relieve symtoms of nausea and help prevent vomiting, which can diminish the effectiveness of orally taken analgesia. In addition some antiemetics such as metoclopramide are prokinetics and help gastric emptying which is often impaired during episodes of migraine. In the UK there are three combination antiemetic and analgesic preparations available: MigraMax (aspirin with metoclopramide), Migraleve (paracetamol/codeine for analgesia, with buclizine as the antiemetic) and paracetamol/metoclopramide (Paramax in UK). The earlier these drugs are taken in the attack, the better their effect.

Some patients find relief from taking other sedative antihistamines which have anti-nausea properties, such as Benadryl which in the US contains diphenhydramine (but a different non-sedative product in the UK).

Serotonin agonists

Sumatriptan and related selective serotonin receptor agonists are excellent for severe migraines or those that do not respond to NSAIDs An open-label study (funded by GelStat) found some tentative evidence of the treatment's effectiveness, but no scientifically sound study has been done.

Comparative studies

Regarding comparative effectiveness of these drugs used to abort migraine attacks, a 2004 placebo-controlled trial reveals that high dose acetylsalicylic acid (1000 mg), sumatriptan 50 mg and ibuprofen 400 mg are equally effective at providing relief from pain, although sumatriptan was superior in terms of the more demanding outcome of rendering patients entirely free of pain and all other migraine-related symptoms.

Another randomized controlled trial, funded by the manufacturer of the study drug, found that a combination of sumatriptan 85 mg and naproxen sodium 200 mg was better than either drug alone.

Preventive treatment

Preventive (also called prophylactic) treatment of migraines can be an important component of migraine management. Such treatments can take many forms, including everything from taking certain drugs or nutritional supplements, to lifestyle alterations such as increased exercise and avoidance of migraine triggers.

The goals of preventive therapy are to reduce the frequency, painfulness, and/or duration of migraines, and to increase the effectiveness of abortive therapy. Another reason to pursue these goals is to avoid medication overuse headache (MOH), otherwise known as rebound headache, which is a common problem among migraneurs. This is believed to occur in part due to overuse of pain medications, and can result in chronic daily headache.

Prescription drugs

A 2006 review article by S. Modi and D. Lowder offers some general guidelines on when a physician should consider prescribing drugs for migraine prevention:

...Therapy should be initiated with medications that have the highest levels of effectiveness and the lowest potential for adverse reactions; these should be started at low dosages and titrated slowly. A full therapeutic trial may take two to six months. After successful therapy (e.g., reduction of migraine frequency by approximately 50 percent or more) has been maintained for six to 12 months, discontinuation of preventive therapy can be considered.

• anticonvulsants such as valproic acid and topiramate. A meta-analysis by the Cochrane Collaboration of ten randomized controlled trials or crossover studies, which together included 1341 patients, found anticonvulsants had an "2.4 times more likely to experience a 50% or greater reduction in frequency with anticonvulsants than with placebo" and a number needed to treat of 3.8. However, concerns have been raised about the marketing of gabapentin.
• antidepressants include tricyclic antidepressants (TCAs) such as amitriptyline and the newer selective serotonin reuptake inhibitors (SSRIs) such as fluoxetine. A meta-analysis by the Cochrane Collaboration found selective serotonin reuptake inhibitors are no more effective than placebo. Another meta-analysis found benefit from SSRIs among patients with migraine or tension headache; however, the effect of SSRIs on only migraines was not separately reported. A randomized controlled trial found that amitriptyline was better than placebo and similar to propranolol.

Other drugs:

• Sansert was withdrawn from the US market by Novartis, but is available in Canadian pharmacies. Although highly effective, it has rare but serious side effects, including retroperitoneal fibrosis.
• Namenda, memantine HCI tablets, which is used in the treatment of Alzheimer's Disease, is beginning to be used off label for the treatment of migraines. It has not yet been approved by the FDA for the treatment of migraines.
• ASA or Asprin can be taken daily in low doses such as 80 to 81 mg, the blood thinners in ASA has been shown to help some migrainures, especially those who have an aura.

Trigger avoidance

Patients can attempt to identify and avoid factors that promote or precipitate migraine episodes. Moderation in alcohol and caffeine intake, consistency in sleep habits, and regular meals may be helpful. General dietary restriction has not been demonstrated to be an effective approach to treating migraine, and migraine is remarkably resistant to the placebo effect http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=15806385&query_hl=8&itool=pubmed_docsum

Herbal and nutritional supplements

Butterbur

50 mg or 75 mg/day of butterbur (Petasites hybridus) rhizome extract was shown in a controlled trial to provide 50% or more reduction in the number of migraines to 68% of participants in the 75 mg dose group, 56% in the 50 mg dose group and 49% in the placebo group after four months. Native butterbur contains some carcinogenic compounds, but a purified version, Petadolex, does not.http://www.webmd.com/content/article/98/105003.htm?z=1728_00000_1000_tn_04

Cannabis

Cannabis was a standard treatment for migraines from the mid-19th century until it was outlawed in the early 20th century in the USA. It has been reported to help people through an attack by relieving the nausea and dulling the head pain, as well as possibly preventing the headache completely when used as soon as possible after the onset of pre-migraine symptoms, such as aura. There is some indication that semi-regular use may reduce the frequency of attacks. Further studies are being conducted. Some migraine sufferers report that cannabis decreases throbbing and pain, especially if smoked. A pharmaceutical company is currently conducting trials of a whole cannabis extract spray for migrainehttp://www.gwpharm.com/research_migraine_removed.asp

Coenzyme Q10

Supplementation of coenzyme Q10 has been found to have a beneficial effect on the condition of some sufferers of migraines. In an open-label trial, Young and Silberstein found that 61.3% of patients treated with 100 mg/day had a greater than 50% reduction in number of days with migraine, making it more effective than most prescription prophylactics. Fewer than 1% reported any side effects. A double-blind placebo-controlled trial has also found positive results.

Feverfew

The plant feverfew (Tanacetum parthenium) is a traditional herbal remedy believed to reduce the frequency of migraine attacks. A number of clinical trials have been carried out to test this claim, but a 2004 review article concluded that the results have been contradictory and inconclusive. However, since then, more studies have been carried out. As well as its prophylactic properties, feverfew is also touted as a migraine abortative.

Magnesium Citrate

Magnesium citrate has reduced the frequency of migraine in an experiment in which the magnesium citrate group received 600 mg per day oral of trimagnesium dicitrate. In weeks 9–12, the frequency of attacks was reduced by 41.6% in the magnesium citrate group and by 15.8% in the placebo group.

Riboflavin

The supplement Riboflavin (also called Vitamin B2) has been shown (in a placebo-controlled trial) to reduce the number of migraines, when taken at the high dose of 400 mg daily for three months.

Vitamin B12

There is tentative evidence that Vitamin B12">Vitamin B12Vitamin B12 may be effective in preventing migraines. In particular, in an open-label pilot study, 1 mg of intranasal hydroxocobalamin (a form of Vitamin B12), taken daily for three months, was shown to reduce migraine frequency by 50% or more in 10 of 19 participants. Although the study was not placebo-controlled, this response is larger than the typical placebo effect in migraine prophylaxis.

Surgical treatments

Noninvasive medical treatments

Behavioral treatments

Alternative medicine