Migraine

Migraine
Classification and external resources

The pain of a migraine headache can be debilitating.
ICD-10 G43.
ICD-9 346
OMIM 157300
DiseasesDB 8207 (Migraine)
31876 (Basilar)
4693 (FHM)
MedlinePlus 000709
eMedicine neuro/218 neuro/517 emerg/230 neuro/529
MeSH D008881
Migraines
  • Migraine
  • Prevention of migraines
  • Aura
  • Cortical spreading depression
  • ICHD classification and diagnosis of migraine
    • Retinal migraine
    • Familial hemiplegic migraine
    • Sporadic hemiplegic migraine

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.[1][2] 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".[3]

The typical migraine headache is unilateral (affecting one half of the head) and pulsating, lasting from 4 to 72 hours;[2] symptoms include nausea, vomiting, photophobia (increased sensitivity to light), and phonophobia (increased sensitivity to sound).[4][5][6] Approximately one-third of people who suffer from migraine headaches perceive an aura—unusual visual, olfactory, or other sensory experiences that are a sign that the migraine will soon occur.[7]

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.[8] Studies of twins indicate a 60 to 65 percent genetic influence upon their propensity to develop migraine headache.[9][10] 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.[11]

Contents

Classification

The International Headache Society (IHS) offers guidelines for the classification and diagnosis of migraine headaches, in a document called "The International Classification of Headache Disorders, 2nd edition" (ICHD-2).[12]

According to ICHD-2, there are seven subclasses of migraines (some of which include further subdivisions):

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 person:

  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 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), hot ears, constipation or diarrhea, increased urination, and other visceral symptoms.[13] 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

Screenshot of a YouTube video showing a computer simulation of visual field defects during migraine with aura based on a neural network.[14]

For the 20–30%[15][16] of migraine sufferers who experience 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 (see silent migraine). Symptoms of migraine aura can be visual, sensory, or motor in nature.[17]

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"[18]). 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, gustatory or olfactory hallucinations, temporary dysphasia, vertigo, tingling or numbness of the face and extremities, and hypersensitivity to touch.

Oliver Sacks's book Migraine describes "migrainous deliria" as a result of such intense migraine aura that it is indistinguishable from "free-wheeling states of hallucinosis, illusion, or dreaming."

Visual symptoms of migraine aura

Enhancements reminiscent of a zigzag fort structure

Negative scotoma, loss of awareness of local structures

Positive scotoma, local perception of additional structures

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 sufferer 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, delirium, 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.[19] According to one summary, "Some people feel unusually refreshed or euphoric after an attack, whereas others note depression and malaise."[20]

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:

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
  • Alcohol
  • Menstrual cycle fluctuations, birth control pills, hormone fluctuations during the menopause transition
  • Tension headaches
  • Foods containing tyramine (red wine, aged cheese, smoked fish, chicken livers, figs, and some beans), monosodium glutamate (MSG) or nitrates (like bacon, hot dogs, and salami)
  • Other foods such as chocolate, nuts, peanut butter, avocado, banana, citrus, onions, dairy products, and fermented or pickled foods.
  • long exposures to light from computer screen, video screens, and tv.

– MedlinePlus medical encyclopedia[21]

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 migraine journal 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, e.g., 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. Nightmares or Traumatic Dreams may also be recorded as migraine triggers. 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 and Drink

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

Gluten One 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.[22] 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.[23]

Aspartame While some people believe that aspartame triggers migraines, and anecdotal evidence is present, this has not been medically proven.[24]

MSG MSG is frequently reported as a dietary trigger (12%).[25] In 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.[26][27] However another trial found no effect when 3.5g of MSG was given with food.[28]

Tyramine The National Headache Foundation has a specific list of triggers based on the tyramine theory, detailing allowed, with caution and avoid triggers.[29] However, a 2003 review article concluded that there was no scientific evidence for an effect of tyramine on migraine.[30]

Other A 2005 literature review found that the available information about dietary trigger factors relies mostly on the subjective assessments of patients.[24] 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[31] 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 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.[32] 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.[33]

Other

One study found that for some people who suffer from migraine 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.[34]

Strong fragrances have also been identified as potential triggers, and some sufferers report an increased sensitivity to scent as an aura effect.[35]

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[36] and claimed to have been discredited by others.[37] Trigger points can be at least part of the cause, and perpetuate most kinds of headaches.[38]

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.

A melanopsin-based receptor has been linked to the association between light sensitivity and migraine pain.[39]

Depolarization theory

Animation of cortical spreading depression

A phenomenon known as cortical spreading depression can cause migraines.[40] 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 study in 2007, using the Positron Emission Tomography (PET) technique identified the hypothalamus as being critically involved in the early stages.[41]

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.[36]

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.[36]

The vascular theory of migraines is now seen as secondary to brain dysfunction.[36][42]

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.[36] Triptans activate serotonin receptors to stop a migraine attack.[36]

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.[36]

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 neurogenic inflammation and pain[36]

Diagnosis

Migraines are underdiagnosed[43] and often misdiagnosed.[44] 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":[45]

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.[46]

The presence of either disability, nausea or sensitivity, can diagnose migraine with:[47]

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.[48] 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.[49][50]

Many of the preventive treatments are quite effective: Even with a placebo, one-quarter of patients find that their migraine frequency is reduced by half or more, and actual treatments often far exceed this figure.[51] There are many medicines available to prevent or reduce frequency, duration and severity of migraine attacks. They may also prevent complications of migraine. Propranolol, atenolol, metoprolol, flunarizine, sodium valproate, topiramate, and Nortriptyline are some of the commonly used drugs. But they need to be taken for about 3 months or more.

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%.[52]

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.[27]

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.

Although there is a large number of medications to treat migraine, their effectiveness varies from person to person. What works from one person may not be effective at all for another one, therefore, early intervention becomes very important. Dr. Joel Saper, director of the Michigan Headache and Neurological Institute explains that according to early data untreated headaches can make the person more vulnerable to pain.[53]

Analgesics

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

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.[61]

Analgesics combined with antiemetics

Antiemetics by mouth may help relieve symptoms 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).[62] 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[54] or other over-the-counter drugs.[56] Triptans are a mid-line treatment suitable for many sufferers of typical migraines. They may not work for atypical or unusually severe migraines, transformed migraines, or status (continuous) migraines.

Selective serotonin 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.[52]

Antidepressants

Tricyclic antidepressants have been long established as highly efficacious prophylactic treatments.[52] 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.[52] 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[63] and 5-HT2C receptors[64][65] 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.[52]

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.

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.[66]

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.[67]

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.[68]

Merck Corp is developing a new drug called Telcagepant which is intended to relieve pain without causing vasoconstriction (narrowing of blood vessels) as current medications such as triptans do. Telcagepant would be a safe therapy for migraine suffers with risk factors for cardiovascular disease.[69]

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.[70]

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.[71] An open-label study (funded by GelStat) found some tentative evidence of the treatment's effectiveness,[72] 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.[73]

Cryotherapy and Thermotherapy

During a migraine the blood vessels in the head tend to dilate as a result of many chemical changes in the body. Some believe that these vessels become swollen with blood and thus put pressure on the nerves surrounding the vessels. This pressure causes the nerve to send pain signals to the brain, resulting in the debilitating pain most often associated with migraines. Both heat and cooling therapies uses temperature manipulation to reduce migraine pain. The use of cooling therapy (cyrotherapy) is believed to cause the swollen blood vessels to constrict, thus reducing pulsating migraine pain. The use of thermotherapy, on the other hand, causes blood flow to increase which, in turn, increases the amount of oxygen and nutrients that are sent to the pain site in the brain. Using a product such as SootheAway will allow a migraine sufferer to apply constant temperature therapy to help relieve pain. A recent study published in the Archives of Family Medicine revealed that pressure, heat and cold can help to relieve headache pain.[74]

Exercise

Being a neurological syndrome, tense nerves are normally one of the causes that exacerbate migraine symptoms. Regular exercise is one way to calm nerves.[75] However, this option may be effective for some people but not for others as in some cases it may actually be the cause of migraine. According to Lawrence Newman, MD, director of the Headache Institute at St. Luke's-Roosevelt Hospital Center in New York migraine sufferers have a heightened neurological system which implies that they have a tendency to develop migraine when anything is out of the ordinary. Therefore, such people establish a regular exercise routine. Exercise can benefit them as it releases endorphins, which are the body's natural painkillers, therefore, they can lessen the frequency or severity of migraines.[76]

Comparative studies

Regarding comparative effectiveness of these drugs used to abort migraine attacks, a 2004 placebo-controlled trial[77] 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. [Note that 50 mg of sumatriptan is not a commonly prescribed full dose (100 mg), so would be expected to not be fully comparable.]

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.[54]

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).[78] An initial study by Griffith University on Vitamin B supplements for both prevention and management has yielded promising results.[79]

Medication overuse headaches

Researchers have learned that the brain's biology can change due to the pain and the medications used to treat it.[80] Furthermore, the constant use of over-the-counter or prescription painkillers -two to three days a week after a long period of time- may cause medication-overuse headaches, also known as rebound headaches. Such headache may be recognized by its shifting pattern where the patient experiences migraine-like characteristics and then the symptoms of a tension-type headache. Such shift can occur during the same day.

Substantial evidence has shown that triptans, ergotamines, simple analgesics, opiods, butalbital compounds, vicodin as well as other compounds may cause Medication Overuse Headaches, MOH. To stop MOH, it is necessary to discontinue the medication causing the MOH. However, withdrawal symptoms will be experienced from two to ten days including withdrawal headache, tachycardia, vomiting, anxiety, arterial hypotension, sleep disorders, nervousness, restlessness.[81]

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.[82] 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.[82][83] (Note: Women who experience auras and also take oral contraceptives have an even higher risk of stroke).[3] Migraine sufferers seem to be at risk for both thrombotic and hemorrhagic stroke as well as transient ischemic attacks.[84] 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.[83][85]

Epidemiology

Disability-adjusted life year for migraines per 100,000 inhabitants in 2002.
     no data      less than 45      45-65      65-85      85-105      105-125      125-145      145-165      165-185      185-205      205-225      225-245      more than 245
Age-Gender Incidence

Migraine is an extremely common condition which will affect 12–28% of people at some point in their lives.[1] 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.[1] 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.[86] There is then a rapid growth in incidence amongst girls occurring after puberty,[87][88][89] which continues throughout early adult life.[90] By early middle age, around 25% of women experience a migraine at least once a year, compared with fewer than 10% of men.[1][91] 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%.[1][91]

At all ages, migraine without aura is more common than migraine with aura, with a ratio of between 1.5:1 and 2:1.[92][93] Incidence figures show that the excess of migraine seen in women of reproductive age is mainly due to migraine without aura.[92] Thus in pre-pubertal and post-menopausal populations, migraine with aura is somewhat more common than amongst 15–50 year olds.[90][94]

There is a strong relationship between age, gender and type of migraine.[95]

Geographical differences in migraine prevalence are not marked. Studies in Asia and South America suggest that the rates there are relatively low,[96][97] but they do not fall outside the range of values seen in European and North American studies.[1][91]

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.[98]

History

The Head Ache. George Cruikshank (1819)

Trepanation, the delibrate and (usually) non-fatal drilling of holes into a skull, was practiced 9,000 years ago and earlier.[99] Some scholars have (controversially) speculated that this drastic procedure might have been a migraine treatment, based on cave paintings[100] and on the fact that trepanation was a historical migraine treatment in 17th-century Europe.[99][101] An early written description consistent with migraines is contained in the Ebers papyrus, written around 1200 BC in ancient Egypt.[99]

In 400 BC Hippocrates described the visual aura that can precede the migraine headache and the relief which can occur through vomiting. Aretaeus of Cappadocia 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 bloodletting 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 London 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.[102] 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

  • The City of London Migraine Clinic
  • Migraine Action, a charity dedicated to individuals affected by migraine
  • Migraine Aura Foundation, a German not-for-profit organization
  • Migraine Trust, a British charity

Other

  • Migraine (book), a book by neurologist Oliver Sacks based mainly on his case studies and geared toward the layman
  • Migraine boy, a comic strip featuring a boy with chronic migraine
  • Onze Danses Pour Combattre la Migraine (Eleven Dances for Fighting Migraine), an album by Belgian band Aksak Maboul
  • Treatments for chronic headaches

Footnotes

  1. ↑ 1.0 1.1 1.2 1.3 1.4 1.5 Stovner LJ, Zwart JA, Hagen K, Terwindt GM, Pascual J (April 2006). "Epidemiology of headache in Europe". European Journal of Neurology 13 (4): 333–45. doi:10.1111/j.1468-1331.2006.01184.x. PMID 16643310. 
  2. ↑ 2.0 2.1 The International Classification of Headache Disorders, 2nd Edition
  3. ↑ "Etymology of migraine". Online Etymological Dictionary. http://www.etymonline.com/index.php?term=migraine. Retrieved 27 May 2009. 
  4. ↑ "NINDS Migraine Information Page". National Institute of Neurological Disorders and Stroke, National Institutes of Health. http://www.ninds.nih.gov/disorders/migraine/migraine.htm. Retrieved 2007-06-25. 
  5. ↑ "Advances in Migraine Prophylaxis: Current State of the Art and Future Prospects" (PDF). National Headache Foundation (CME monograph). http://www.headaches.org/pdf/botoxcme.pdf. Retrieved 2007-06-25. 
  6. ↑ Gallagher RM, Cutrer FM (February 2002). "Migraine: diagnosis, management, and new treatment options". The American Journal of Managed Care 8 (3 Suppl): S58–73. PMID 11859906. http://www.ajmc.com/pubMed.php?pii=363. 
  7. ↑ "Guidelines for all healthcare professionals in the diagnosis and management of migraine, tension-type, cluster and medication-overuse headache, January 2007, British Association for the Study of Headache" (PDF). http://216.25.100.131/upload/NS_BASH/BASH_guidelines_2007.pdf. Retrieved 2007-06-25. 
  8. ↑ Ogilvie AD, Russell MB, Dhall P, et al. (January 1998). "Altered allelic distributions of the serotonin transporter gene in migraine without aura and migraine with aura". Cephalalgia 18 (1): 23–6. doi:10.1046/j.1468-2982.1998.1801023.x. PMID 9601620. 
  9. ↑ Gervil M, Ulrich V, Kaprio J, Olesen J, Russell MB (September 1999). "The relative role of genetic and environmental factors in migraine without aura". Neurology 53 (5): 995–9. PMID 10496258. http://www.neurology.org/cgi/pmidlookup?view=long&pmid=10496258. 
  10. ↑ Ulrich V, Gervil M, Kyvik KO, Olesen J, Russell MB (March 1999). "The inheritance of migraine with aura estimated by means of structural equation modelling". Journal of Medical Genetics 36 (3): 225–7. PMID 10204850. PMC 1734315. http://jmg.bmj.com/cgi/pmidlookup?view=long&pmid=10204850. 
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  98. ↑ Ottman R, Lipton RB (1994). "Comorbidity of migraine and epilepsy". Neurology 44 (11): 2105–10. PMID 7969967. 
  99. ↑ 99.0 99.1 99.2 Arulmani, U., "Calcitonin Gene-Related Peptide and Migraine: Implications for Therapy" (2004). Doctoral thesis, Erasmus University. Web-link.
  100. ↑ Brothwell, Don R. (1963). Digging up Bones; the Excavation, Treatment and Study of Human Skeletal Remains. London: British Museum (Natural History). pp. 126. OCLC 14615536. 
  101. ↑ Edmeads, J. (1991). What is migraine? Controversy and stalemate in migraine pathophysiology. J Neurol, 238 Suppl 1, S2-5. DOI weblink.
  102. ↑ Cost of disorders of the brain in Europe

References

Migraine triggers

Treatment

Triptans

General

Economic impact

Clinical picture

External links

General information

Organizations

Pathology of the nervous system, primarily CNS (G04–G47, 323–349)
Inflammation
Encephalitis (Viral encephalitis, Herpesviral encephalitis) · Cavernous sinus thrombosis · Brain abscess (Amoebic)
Myelitis: Poliomyelitis · Demyelinating disease (Transverse myelitis) · Tropical spastic paraparesis · Epidural abscess
Both/either
Encephalomyelitis (Acute disseminated)
Meningoencephalitis
Brain/
encephalopathy
Degenerative
Extrapyramidal and
movement disorders

Basal ganglia disease: Parkinsonism (PD, Postencephalitic, NMS) · PKAN · Tauopathy (PSP) · Striatonigral degeneration · Hemiballismus · HD · OA

Dyskinesia: Dystonia (Status dystonicus, Spasmodic torticollis, Meige's, Blepharospasm) · Chorea (Choreoathetosis) · Myoclonus (Myoclonic epilepsy) · Akathesia

Tremor (Essential tremor, Intention tremor) · Restless legs · Stiff person

Tauopathy: Alzheimer's (Early-onset) · Frontotemporal dementia/Frontotemporal lobar degeneration (Pick's, Dementia with Lewy bodies)

Multi-infarct dementia
Leigh's
Demyelinating
autoimmune (Multiple sclerosis, Neuromyelitis optica, Schilder's disease) · hereditary (Adrenoleukodystrophy, Alexander, Canavan, Krabbe, ML, PMD, VWM, MFC, CAMFAK syndrome) · Central pontine myelinolysis · Marchiafava-Bignami disease · Alpers' disease
Episodic/
paroxysmal
Focal · Generalised · Status epilepticus · Myoclonic epilepsy
Migraine (Familial hemiplegic) · Cluster · Tension
Cerebrovascular
TIA (Amaurosis fugax, Transient global amnesia)
Stroke (MCA, ACA, PCA, Foville's, Millard-Gubler, Lateral medullary, Weber's, Lacunar stroke)
Insomnia · Hypersomnia · Sleep apnea (Obstructive, Ondine's curse) · Narcolepsy · Cataplexy · Kleine-Levin · Circadian rhythm sleep disorder (Advanced sleep phase syndrome, Delayed sleep phase syndrome, Non-24-hour sleep-wake syndrome, Jet lag)
Intracranial hypertension (Hydrocephalus/NPH, Idiopathic intracranial hypertension) · Cerebral edema · Intracranial hypotension
Other
Brain herniation · Reye's · Hepatic encephalopathy · Toxic encephalopathy
Spinal cord/
myelopathy
Syringomyelia · Syringobulbia · Morvan's syndrome · Vascular myelopathy (Foix-Alajouanine syndrome) · Spinal cord compression
Both/either
Degenerative
SA
Friedreich's ataxia · Ataxia telangiectasia

UMN only: PLS · PP · HSP

LMN only: PMA · PBP (Fazio-Londe, Infantile progressive bulbar palsy) · SMA (SMN-linked, Kennedy disease, SMAX2, DSMA1)

both: ALS

: CNS

anat(s,m,p,,e,b,d,c,,f,,g)/phys/devp/cell

noco(m,d,e,h,v,s)/cong/tumr,sysi/,injr

proc,drug(N1A/2AB/C/3/4/7A/B//)
CNS disease: Headache (G43-G44, 339, 346)
Primary
ICHD 1
Migraine (Familial hemiplegic) · Retinal migraine
ICHD 2
Tension
ICHD 3
Cluster · Chronic paroxysmal hemicrania
ICHD 4
Hemicrania continua · Thunderclap headache · Coital cephalalgia · New daily persistent headache · Hypnic headache
Secondary
ICHD 7
Ictal headache · Post dural puncture headache
ICHD 8
Hangover · Medication overuse headache
ICHD 13
Trigeminal neuralgia · Occipital neuralgia · External compression headache · Cold-stimulus headache · Optic neuritis · Postherpetic neuralgia · Tolosa-Hunt syndrome
Other
Vascular

: CNS

anat(s,m,p,,e,b,d,c,,f,,g)/phys/devp/cell

noco(m,d,e,h,v,s)/cong/tumr,sysi/,injr

proc,drug(N1A/2AB/C/3/4/7A/B//)
Antimigraine preparations (N02C)
Analgesic/abortive
Serotonin modulators
Ergot alkaloids
Dihydroergotamine • Ergotamine • Methysergide • Lisuride
5-HT1 agonists
Triptans (Almotriptan, Avitriptan, Eletriptan, Frovatriptan, Naratriptan, Rizatriptan, Sumatriptan, Zolmitriptan) Alniditan
Other
Dotarizine
Other
Paracetamol# • Amidrine
Prevention of migraines
Propranolol# • Timolol
verapamil
corticosteroid
flumedroxone
monosaccharide
topiramate
adrenergic agonist
amitriptyline • nortriptyline • imipramine
valproate • carbamazepine • oxcarbazepine
Ungrouped
piperidine (Pizotifen) • adrenochrome (Iprazochrome) • phenothiazine (Dimetotiazine) • benzoxepin (Oxetorone) • piperazine (Lomerizine) • azepine (Telcagepant)
#WHO-EM. ‡Withdrawn from market. Clinical trials: †Phase III. §Never to phase III

: CNS

anat(s,m,p,,e,b,d,c,,f,,g)/phys/devp/cell

noco(m,d,e,h,v,s)/cong/tumr,sysi/,injr

proc,drug(N1A/2AB/C/3/4/7A/B//)