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Migraine is a neurological syndrome characterized by altered bodily perceptions, severe headaches, and nausea. Physiologically, the migraine headache is a neurological condition more common to women than to men . The word migraine was borrowed from Old French migraigne (originally as "megrim", but respelled in 1777 on a contemporary French model). The French term derived from a vulgar pronunciation of the Late Latin word hemicrania, itself based on Greek hemikrania, from Greek roots for "half" and "skull".

The typical migraine headache is unilateral and pulsating, lasting from 4 to 72 hours; symptoms include nausea, vomiting, photophobia (increased sensitivity to light), and phonophobia (increased sensitivity to sound). Approximately one-third of people who suffer migraine headache perceive an aura—unusual visual, olfactory, or other sensory experiences that are a sign that the migraine will soon occur.

Initial treatment is with analgesics for the headache, an antiemetic for the nausea, and the avoidance of triggering conditions. The cause of migraine headache is unknown; the most common theory is a disorder of the serotonergic control system.

There are migraine headache variants, some originate in the brainstem (featuring intercellular transport dysfunction of calcium and potassium ions) and some are genetically disposed. Studies of twins indicate a 60 to 65 percent genetic influence upon their propensity to develop migraine headache. Moreover, fluctuating hormone levels indicate a migraine relation: 75 percent of adult patients are women, although migraine affects approximately equal numbers of prepubescent boys and girls; propensity to migraine headache is known to disappear during pregnancy, although in some women migraines may become more frequent during pregnancy.

Classification

The International Headache Society (IHS) classifies migraine headache.

Defining pain severity

The IHS defines the intensity of pain with a verbal, four-point scale:
Number Name Annotations
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


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 40–60% 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 visceral 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 nose-mouth area on the same side. 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.

File:Fortifikation (Migräne).jpg|Enhancements reminiscent of a zigzag fort structureFile:Negatives Skotom (Brandenburger Tor Blaue Stunde) 1.jpg|Negative scotoma, loss of awareness of local structuresFile:Positives Skotom (Brandenburger Tor Blaue Stunde) 1.jpg|Positive scotoma, local perception of additional structuresFile:Gesichtsfeldausfall (Brandenburger Tor Blaue Stunde) 1.jpg|Mostly one-sided loss of perception

Pain phase

The typical migraine headache is unilateral, throbbing, and moderate to severe and can be aggravated by physical activity. Not all these features are necessary. The pain may be bilateral at the onset or start on one side and become generalized, and usually it alternates sides from one attack to the next. The onset is usually gradual. The pain peaks and then subsides and usually lasts 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 a week, and the average migraineur experiences 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, and vomiting occurs in about one third of patients. Many patients experience sensory hyperexcitability manifested by photophobia, phonophobia, and 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. The extremities tend to feel cold and moist. Vertigo may be experienced; a variation of the typical migraine, called vestibular migraine, has also been described. Lightheadedness, rather than true vertigo, and a feeling of faintness may occur.

Postdrome phase

The patient may feel tired or "hungover" and have head pain, cognitive difficulties, gastrointestinal symptoms, mood changes, and weakness. 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. For some patients, a 5- to 6-hour nap may reduce the pain, but slight headaches may still occur when the patient stands or sits quickly. These symptoms may go away after a good night's rest, although there is no guarantee. Some people may suffer and recover differently than others.

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.'

The MedlinePlus Medical Encyclopedia, for example, offers the following list of migraine triggers:

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 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

Many migraine sufferers report reduced incidence of migraines due to identifying and avoiding their individual food triggers. However, more studies are needed.

GlutenOne food elimination that has proven to reduce or eliminate migraines in a percentage of patients is gluten. For those with (often undiagnosed) celiac disease or other forms of gluten sensitivity, migraines may be a symptom of gluten intolerance. One study found that migraine sufferers were ten times more likely than the general population to have celiac disease, and that a gluten-free diet eliminated or reduced migraines in these patients. Another study of 10 patients with a long history of chronic headaches that had recently worsened or were resistant to treatment found that all 10 patients were sensitive to gluten. MRI scans determined that each had inflammation in their central nervous systems caused by gluten-sensitivity. Seven out of nine of these patients that went on a gluten-free diet stopped having headaches completely.

AspartameWhile some people believe that aspartame triggers migraines, and anecdotal evidence is present, this has not been medically proven.

MSGIn a placebo-controlled trial, monosodium glutamate (MSG) in large doses (2.5 grams) taken on an empty stomach was associated with adverse symptoms including headache more often than was placebo. However another trial found no effect when 3.5g of MSG was given with food.

TyramineThe National Headache Foundation has a specific list of triggers based on the tyramine theory, detailing allowed, with caution and avoid triggers. However, a 2003 review article concluded that there was no scientific evidence for an effect of tyramine on migraine.

OtherA 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. However, 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.

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.

Other

One study found that for some migraineurs in India, washing hair in a bath was a migraine trigger. The triggering effect also had to do with how the hair was later dried.

Strong fragrances have also been identified as potential triggers, and some sufferers report an increased sensitivity to scent as an aura effect.

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. Trigger points can be at least part of the cause, and perpetuate most kinds of headaches.

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.

When the constriction stops and the blood vessels dilate, they become too wide. The once solid walls of the blood vessels become permeable and some fluid leaks out. This leakage is recognized by pain receptors in the blood vessels of surrounding tissue. In response, the body supplies the area with chemicals which cause inflammation. With each heart beat, blood passes through this sensitive area causing a throb of pain.

The vascular theory of migraines is now seen as secondary to brain dysfunction.

Serotonin theory

Serotonin is a type of neurotransmitter, or "communication chemical" which passes messages between nerve cells. It helps to control mood, pain sensation, sexual behaviour, sleep, as well as dilation and constriction of the blood vessels among other things. Low serotonin levels in the brain may lead to a process of constriction and dilation of the blood vessels which trigger a migraine. Triptans activate serotonin receptors to stop a migraine attack.

Neural theory

When certain nerves or an area in the brain stem become irritated, a migraine begins. In response to the irritation, the body releases chemicals which cause inflammation of the blood vessels. These chemicals cause further irritation of the nerves and blood vessels and results in pain. Substance P is one of the substances released with first irritation. Pain then increases because substance P aids in sending pain signals to the brain.

Unifying theory

Both vascular and neural influences cause migraines.
  1. stress triggers changes in the brain
  2. these changes cause serotonin to be released
  3. blood vessels constrict and dilate
  4. chemicals including substance P irritate nerves and blood vessels causing pain


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:

Migraine should be differentiated from other causes of headaches such as cluster headaches. These are extremely painful, unilateral headaches of a piercing quality. The duration of the common attack is 15 minutes to three hours. Onset of an attack is rapid, and most often without the preliminary signs that are characteristic of a migraine.

Prevention

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.

Many of the preventive treatments are quite effective: Even with a placebo (sham treatment), one-quarter of patients find that their migraine frequency is reduced by half or more, and actual treatments often far exceed this figure.

Management

Conventional treatment focuses on three areas: trigger avoidance, symptomatic control, and prophylactic pharmacological drugs. Patients who experience migraines often find that the recommended migraine treatments are not 100% effective at preventing migraines, and sometimes may not be effective at all. Pharmacological treatments are considered effective if they reduce the frequency or severity of migraine attacks by 50%.

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.

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 (known as acetaminophen in North America) 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. Excedrin is an example of an aspirin with caffeine product. Caffeine is recognized by the U.S. Food and Drug Administration as an Over The Counter Drug (OTC) treatment for migraine when compounded with aspirin and paracetamol. Even by itself, caffeine can be helpful during an attack, despite the fact that in general migraine-sufferers are advised to limit their caffeine intake.


Patients themselves often start off with paracetamol, 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.

In all, the U.S. Food and Drug Administration has approved three OTC products specifically for migraine: Excedrin Migraine, Advil Migraine, and Motrin Migraine Pain. Excedrin Migraine, as mentioned above, is a combination of aspirin, acetaminophen, and caffeine. Both Advil Migraine and Motrin Migraine Pain are straight NSAIDs, with ibuprofen as the only active ingredient.

Analgesics combined with antiemetics

Antiemetics 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 or other over-the-counter drugs. Triptans are a mid-line treatment suitable for many migraineurs with typical migraines. They may not work for atypical or unusually severe migraines, transformed migraines, or status (continuous) migraines.

Serotonin specific reuptake inhibitors (SSRIs) are not approved by the U.S. Food and Drug Administration (FDA) for treatment of migraines, but have been found to be effective by clinical consensus.

Antidepressants

Tricyclic antidepressants have been long established as highly efficacious prophylactic treatments. These drugs, however, may give rise to undesirable side effects, such as insomnia, sedation or sexual dysfunction. SSRIs antidepressants are less established than tricyclics for migraines prophylaxis. Despite the absence of FDA approval for migraine treatment, antidepressants are widely prescribed. In addition to tricyclics and SSRIs, the anti-depressant nefazodone may also be beneficial in the prophylaxis of migraines due to its antagonistic effects on the 5-HT2A and 5-HT2C receptors It has a more favorable side effect profile than amitriptyline, a tricyclic antidepressant commonly used for migraine prophylaxis. Anti-depressants offer advantages for treating migraine patients with comorbid depression.

Ergot alkaloids

Until the introduction of sumatriptan in 1991, ergot derivatives (see ergoline) were the primary oral drugs available to abort a migraine once it is established.

Ergot drugs can be used either as a preventive or abortive therapy, though their relative expense and cumulative side effects suggest reserving them as an abortive rescue medicine. However, ergotamine tartrate tablets (usually with caffeine), though highly effective, and long lasting (unlike triptans), have fallen out of favour due to the problem of ergotism. Oral ergotamine tablet absorption is reliable unless the patient is nauseated. Anti-nausea administration is available by ergotamine suppository (or Ergostat sublingual tablets made until circa 1992). Ergot drugs themselves can be so nauseating it is advisable for the sufferer to have something at hand to counteract this effect when first using this drug. Ergotamine-caffeine 1/100 mg fixed ratio tablets (like Cafergot, Ercaf, etc.) are much less expensive per headache than triptans, and are commonly available in Asia and Romania (Cofedol). They are difficult to obtain in the USA. Ergotamine-caffeine can't be regularly used to abort evening or night onset migraines due to debilitating caffeine interference with sleep. Pure ergotamine tartrate is highly effective for evening-night migraines, but is rarely or never available in the USA. Dihydroergotamine (DHE), which must be injected or inhaled, can be as effective as ergotamine tartrate, but is much more expensive than $2 USD Cafergot tablets.

Low-dose psychedelics
Many anecdotes indicate that LSD, ergine, (and the related compounds in psychedelic mushrooms, psilocybin & psilocin, although they are not ergot alkaloids) are effective in preventing and treating migraines as well as cluster headaches. The doses do not have to be high enough to cause psychedelic effects to have an effect on migraines.

Steroids

Based on a recent meta analysis a single dose of IV dexamethasone, when added to standard treatment, is associated with a 26% decrease in headache recurrence.

Other agents

If over-the-counter medications do not work, or if triptans are unaffordable, the next step for many doctors is to prescribe Fioricet or Fiorinal, which is a combination of butalbital (a barbiturate), paracetamol (in Fioricet) or acetylsalicylic acid (more commonly known as aspirin and present in Fiorinal), and caffeine. While the risk of addiction is low, butalbital can be habit-forming if used daily, and it can also lead to rebound headaches. Barbiturate-containing medications are not available in many European countries.

Amidrine, Duradrin, and Midrin is a combination of acetaminophen, dichloralphenazone, and isometheptene often prescribed for migraine headaches. Some studies have recently shown that these drugs may work better than sumatriptan for treating migraines.

Antiemetics may need to be given by suppository or injection where vomiting dominates the symptoms.

Recently it has been found that calcitonin gene related peptides (CGRPs) play a role in the pathogenesis of the pain associated with migraine as triptans also decrease its release and action. CGRP receptor antagonists such as olcegepant and telcagepant are being investigated both in vitro and in clinical studies for the treatment of migraine.

Status migrainosus
Status migrainosus is characterized by migraine lasting more than 72 hours, with not more than four hours of relief during that period. It is generally understood that status migrainosus has been refractory to usual outpatient management upon presentation.

Treatment of status migrainosus consists of managing comorbidities (i. e. correcting fluid and electrolyte abnormalities resulting from anorexia and nausea/vomiting often accompanying status migr.), and usually administering parenteral medication to "break" (abort) the headache.

Although the literature is full of many case reports concerning treatment of status migrainosus, first line therapy consists of intravenous fluids, metoclopramide, and triptans or DHE.

Herbal treatment
The herbal supplement feverfew (more commonly used for migraine prevention, see below) is marketed by the GelStat Corporation as an OTC migraine abortive, administered sublingually (under the tongue) in a mixture with ginger. An open-label study (funded by GelStat) found some tentative evidence of the treatment's effectiveness, but no scientifically sound study has been done. Cannabis, in addition to prevention, is also known to relieve pain during the onset of a migraine.

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.

Recently the combination of sumatriptan 85 mg and naproxen sodium 500 mg was demonstrated to be effective and well tolerated in an early intervention paradigm for the acute treatment of migraine. Significant pain-free responses in favor of sumatriptan/naproxen were demonstrated as early as 30 minutes, maintained at 1 hour, and sustained from 2 to 24 hours. At 2 and 4 hours, sumatriptan/naproxen provided significantly lower rates of traditional migraine-associated symptoms (nausea, photophobia, and phonophobia) and nontraditional migraine-associated symptoms (neck pain/discomfort and sinus pain/pressure).

Prognosis

Cardiovascular risks

The risk of stroke may be increased two- to threefold in migraine sufferers. Young adult sufferers and women using hormonal contraception appear to be at particular risk. The mechanism of any association is unclear, but chronic abnormalities of cerebral blood vessel tone may be involved. Women who experience auras have been found to have twice the risk of strokes and heart attacks over non-aura migraine sufferers and women who do not have migraines. Migraine sufferers seem to be at risk for both thrombotic and hemorrhagic stroke as well as transient ischemic attacks. Death from cardiovascular causes was higher in people with migraine with aura in a Women's Health Initiative study, but more research is needed to confirm this.

Epidemiology

[[Image:Migraine world map - DALY - WHO2002.svg|thumb|Disability-adjusted life year for migraines per 100,000 inhabitants in 2002.


]]
Age-Gender Incidence
Migraine is an extremely common condition which will affect 12–28% of people at some point in their lives. 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. These figures vary substantially with age: approximately 4–5% of children aged under 12 suffer from migraine, with little apparent difference between boys and girls. 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%.

At all ages, migraine without aura is more common than migraine with aura, with a ratio of between 1.5:1 and 2:1. Incidence figures show that the excess of migraine seen in women of reproductive age is mainly due to migraine without aura. Thus in pre-pubertal and post-menopausal populations, migraine with aura is somewhat more common than amongst 15–50 year olds.

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.

The incidence of migraine is related to the incidence of epilepsy in families, with migraine twice as prevalent in family members of epilepsy sufferers, and more common in epilepsy sufferers themselves.

History

9,000 year old skulls exist with evidence of trepanation. It is hypothesized that this drastic step was taken in response to headaches, though there is no clear evidence proving this. . Headache with neuralgia was recorded in the medical documents of the ancient Egyptians as early as 1200 BC.

In 400 BC Hippocrates described the visual aura that can precede the migraine headache and the relief which can occur through vomiting. Aretaeus of Cappadociamarker is credited as the "discoverer" of migraines because of his second century description of the symptoms of a unilateral headache associated with vomiting, with headache-free intervals in between attacks.

Galenus of Pergamon used the term "hemicrania" (half-head), from which the word "migraine" was derived. He thought there was a connection between the stomach and the brain because of the nausea and vomiting that often accompany an attack. For relief of migraine, Andalusian-born physician Abulcasis, also known as Abu El Qasim, suggested application of a hot iron to the head or insertion of garlic into an incision made in the temple.

In the Middle Ages migraine was recognized as a discrete medical disorder with treatment ranging from hot irons to blood letting and even witchcraft . Followers of Galenus explained migraine as caused by aggressive yellow bile.Ebn Sina (Avicenna) described migraine in his textbook "El Qanoon fel teb" as "... small movements, drinking and eating, and sounds provoke the pain... the patient cannot tolerate the sound of speaking and light. He would like to rest in darkness alone."Abu Bakr Mohamed Ibn Zakariya Râzi noted the association of headache with different events in the lives of women, "...And such a headache may be observed after delivery and abortion or during menopause and dysmenorrhea."

In Bibliotheca Anatomica, Medic, Chirurgica, published in Londonmarker in 1712, five major types of headaches are described, including the "Megrim", recognizable as classic migraine.Graham and Wolff (1938) published their paper advocating ergotamine tart for relieving migraine. Later in the 20th century, Harold Wolff (1950) developed the experimental approach to the study of headache and elaborated the vascular theory of migraine, which has come under attack as the pendulum again swings to the neurogenic theory.

Society and culture

Economic impact

In addition to being a major cause of pain and suffering, chronic migraine attacks are a significant source of both medical costs and lost productivity.It has been estimated to be the most costly neurological disorder in the European Community, costing more than €27 billion per year. Medical costs per migraine sufferer (mostly physician and emergency room visits) averaged $107 USD over six months in one 1988 study, with total costs including lost productivity averaging $313. Annual employer cost of lost productivity due to migraines was estimated at $3,309 per sufferer. Total medical costs associated with migraines in the United States amounted to one billion dollars in 1994, in addition to lost productivity estimated at thirteen to seventeen billion dollars per year. Employers may benefit from educating themselves on the effects of migraines in order to facilitate a better understanding in the workplace. The workplace model of 9–5, 5 days a week may not be viable for a migraine sufferer. With education and understanding an employer could compromise with an employee to create a workable solution for both.

See also



Organizations



Other



Footnotes

  1. The International Classification of Headache Disorders, 2nd Edition
  2. Complete supplement online
  3. Complete supplement online (see page 150)
  4. link titleMigraine Linked to Celiac Disease
  5. Migraine Headaches: Gluten Triggers Severe Headaches in Sensitive Individuals
  6. link titleFragrance Migraine Triggers
  7. Trigger Point Therapy for Headaches & Migraines, DeLaune, Valerie (New Harbinger: 2008) [1]
  8. http://ecfr.gpoaccess.gov/cgi/t/text/text-idx?c=ecfr&sid=a00605d20ab938aed6a579c5c6d2f5c5&rgn=div6&view=text&node=38:1.0.1.1.5.2&idno=38
  9. "Migraine headaches" information from the Cleveland Clinic
  10. Mayo Clinic Proceedings 1996;71:1055-1066
  11. Saper JR, Lake AE, Tepper SJ.(2001) "Nefazodone for chronic daily headache prophylaxis: an open-label study." Headache. 2001 May;41(5):465-74.PMID: 11380644
  12. Mylecharane EJ.(1991)"5-HT2 receptor antagonists and migraine therapy."1: J Neurol. 1991;238 Suppl 1:S45-52.PMID: 2045831
  13. Millan MJ.(2005)"Serotonin 5-HT2C receptors as a target for the treatment of depressive and anxious states: focus on novel therapeutic strategies." 2005 Sep-Oct;60(5):441-60. PMID: 16433010
  14. Freitag, Frederick G., Cady, Roger, DiSerio, Frank, Elkind, Arthur, Gallagher, R. Michael, Goldstein, Jerome, Klapper, Jack A., Rapoport, Alan M., Sadowsky, Carl, Saper, Joel R. & Smith, Timothy R. "Comparative Study of a Combination of Isometheptene Mucate, Dichloralphenazone With Acetaminophen and Sumatriptan Succinate in the Treatment of Migraine." Headache: The Journal of Head and Face Pain 41 (4), 391-398.
  15. UpToDate.
  16. Migraine News for February 2005, accessed January 4, 2008
  17. See also summary poster.
  18. Russo, Ethan (1998). Cannabis for migraine treatment: the once and future prescription? An historical and scientific review. Pain 76:3-8.
  19. Etminan M, Takkouche B, Isorna FC, et al. Risk of ischaemic stroke in people with migraine: Systematic review and meta-analysis of observational studies. BMJ. 2005;330:63. PMID 15596418
  20. Becker C, Brobert GP, Almqvist PM, Johansson S, Jick SS, Meier CR. Migraine and the risk of stroke, TIA, or death in the UK (CME). Headache. 2007;47(10):1374–84. PMID 18052947
  21. Waters WE, Campbell MJ, Elwood PC. Migraine, headache, and survival in women. BMJ (Clin Res Ed). 1983;287:1442–1443. PMID 6416449
  22. Cost of disorders of the brain in Europe


References

Migraine triggers

  • Federation of American Societies for Experimental Biology [FASEB] [1995]. Analysis of adverse reactions to monosodium glutamate (MSG). Bethesda, MD: Life Sciences Research Office, FASEB.


  • Ravishankar, K (2006). 'Hair wash' or 'Head bath' triggering migraine - observations in 94 Indian patients". Cephalagia 26 (11): 1330–1334. ISSN 0333-1024.


Treatment

  • Pearce, J.M.S. (1994). Headache. Neurological Management series. Journal of Neurology Neurosurgery and Psychiatry. 57, 134–144.
  • Mayo Clinic Staff. (2005). Migraine Headache. Retrieved August 14, 2005
  • Cathy Wong, ND. (2005). Migraine Elimination Diet Retrieved August 14, 2005
  • Treatment Articles (2005). Butterbur, Co-enzyme Q-10, Melatonin, Folic Acid
  • Buchholz, D. (2002) Heal your headache: The 1-2-3 Program, New York: Workman Publishing, ISBN 0-7611-2566-3
  • Livingstone, I. and Novak, D. (2003) Breaking the Headache Cycle, New York: Henry Holt and Co. ISBN 0-8050-7221-7
  • Izecksohn L, and Izecksohn C. . Fluids' Hypertension Syndromes, ISBN 978-85-906664-0-0.


Triptans

  • Cohen JA, Beall D, Beck A, et al. Sumatriptan treatment for migraine in a health maintenenace organization: economic, humanistic, and clinical outcomes. Clin Ther 1999;21:190–205.
  • Adelman JU, Sharfman M, Johnson R, et al. Impact of oral sumatriptan on workplace productivity, health-related quality of life, healthcare use, and patient satisfaction with medication in nurses with migraine. Am J Manag Care 1996;2:1407–1416.
  • Cohen JA, Beall DG, Miller DW, Beck A, Pait G, Clements BD. Subcutaneous sumatriptan for the treatment of migraine: humanistic, economic, and clinical consequences. Fam Med 1996;28:171–177.
  • Jhingran P, Cady RK, Rubino J, Miller D, Grice RB, Gutterman DL. Improvements in health-related quality of life with sumatriptan treatment for migraine. J Med Econ 1996;42:36–42.
  • Solomon GD, Nielsen K, Miller D. The effects of sumatriptan on migraine: health-related quality of life. Med Interface 1995;June:134–141.
  • Solomon GD, Skobieranda FG, Genzen JR. Quality of life assessment among migraine patients treated with sumatriptan. Headache 1995;35:449–454.
  • Santanello NC, Polis AB, Hartmaier SL, Kramer MS, Block GA, Silberstein SD. Improvement in migrainespecific quality of life in a clinical trial of rizatriptan. Cephalalgia 1997;17:867–872.
  • Caro JJ, Getsios D. Pharmacoeconomic evidence and considerations for triptan treatment of migraine. Expert Opin Pharmacother 2002;3:237–248.
  • Lofland JH, Johnson NE, Batenhorst AS, Nash DB. Changes in resource use and outcomes for patients with migraine treated with sumatriptan: a managed care perspective. Arch Intern Med 1999;159: 857–863.
  • Cady RC, Ryan R, Jhingran P, O’Quinn S, Pait DG. Sumatriptan injection reduces productivity loss during a migraine attack. Arch Intern Med 1998;158: 1013–1018.
  • Litaker DG, Solomon GD, Genzen JR. Impact of sumatriptan on clinic utilization and costs of care in migraineurs. Headache 1996;36:538–541.
  • Greiner DL, Addy SN. Sumatriptan use in a large group-model health maintenance organization. Am J Health Syst Pharm 1996;53:633–638.
  • Lofland JH, Kim SS, Batenhorst AS, et al. Cost-effectiveness and cost-benefit of sumatriptan in patients with migraine. Mayo Clin Proc 2001;76:1093–1101.
  • Biddle AK, Shih YC, Kwong WJ. Cost-benefit analysis of sumatriptan tablets versus usual therapy for treatment of migraine. Pharmacotherapy 2000;20: 1356–1364.
  • Caro JJ, Getsios D, Raggio G, Caro G, Black L. Treatment of migraine in Canada with naratriptan: a costeffectiveness analysis. Headache 2001;41:456–464.


General

  • Sacks, Oliver (1999) Migraine, Vintage ISBN 0-520-08223-0
  • Relouzat, Raoul & Thiollet, Jean-Pierre, Vaincre la migraine, Anagramme, 2006 ISBN 2-35035046
  • Blondin, Betsy, (2008) "Migraine Expressions: A Creative Journey through Life with Migraine, WordMetro Press ISBN 0615201970


Economic impact

  • Edmeads J, Mackell JA. The economic impact of migraine: an analysis of direct and indirect costs. Headache 2002;42:501–509.
  • Gerth WC, Carides GW, Dasbach EJ, Visser WH, Santanello NC. The multinational impact of migraine symptoms on healthcare utilisation and work loss. Pharmacoeconomics 2001;19:197–206.
  • Hu XH, Markson LE, Lipton RB, Stewart WF, Berger ML. Burden of migraine in the United States: disability and economic costs. Arch Intern Med 1999;159:813–818.
  • Osterhaus JT, Gutterman DL, Plachetka JR. Healthcare resource and low labour costs of migraine headaches in the US. Pharmacoeconomics 1992;2:2–11.


Clinical picture

  • Blau JN. Classical migraine: symptoms between visual aura and headache onset. Lancet 1992;340:355-6.
  • Silberstein SD: Migraine symptoms: Results of a survey of self-reported migraineurs. Headache 1995;35:387-96.
  • Silberstein SD, Saper JR, Freitag F. Migraine: Diagnosis and treatment. In: Silberstein SD, Lipton RB, Dalessio DJ, eds. Wolff's headache and other head pain. 7th ed. New York: Oxford University Press, 2001:121–237.


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